Exam 1 Flashcards
-itis
inflammation
-osis
degeneration
–oma, -trophy, -plasia
disorders of growth
-opathy
uncertain pathogenesis
what causes enlargement of cells
glycogen
hypertrophy of organelles
storage changes/error in metabolism (e.g. lysosomal storage disease
hyaline
homogenous, glossy appearance
describes IC proteins depositions (russel bodies, metal inclusions, viral inclusions)
describes EC protein deposits (edema fluid, fibrin, amyloid)
causes of amyloid
EC protein deposits composed of protein fibrils in beta pleated sheet
AA Amyloid
serum amyloid A
AL Amyloid
Ig light chains
AF Amyloid
prealbumin
endocrine amyloid
hormone and hormone-like proteins
type of amyloid in glomeruli in dogs, hepatic sinusoids in birds
AA amyloid
type of amyloid in lymphoid follicles
AL amyloid
type of amyloid in pancreatic islets or renal medulla in cats
endocrine amyloid
biochemical features of amyloid
insoluble
indigestable
morphological features of amyloid
amorphous
hyaline
extracellular
stains red/orange with congo red
stains green with Thioflavine T
Some parenchymal cells have a few small round, perfectly clear cytoplasmic spaces
reversible fatty change
All parenchymal cells contain a very large, perfectly clear, round cytoplasmic space
irreversible fatty degeneration
Some parenchymal cells have modest cytoplasmic swelling
reversible hydropic change
All parenchymal cells are markedly swollen
irreversible hydropic degeneration
pyknosis
shrinkage, clumping of nuclear chromatin
karyorrhexis
nuclear fragmentations
karyolysis
nuclear fading
Pro-Oxidants
xanthine oxidase
fenton & haber weiss reactions
superoxide anion, singlet oxygen
hydroxyl radical
nitric oxide
hydrogen peroxide
anti-oxidants
superoxide dismutase & catalase
glutathione peroxidase/reductase
vitamins A,C,E
transferrin, lactoferrin, ceruloplasmin
ATP depletion role in cell injury
affects membrane transport, protein synthesis, lipogenesis, phospholipid turner, and metabolism
Ca influx role in cell injury
activates enzymes (phospholipases, proteases, ATPases, endonucleases)
mitochondrial injury role in cell injury
mitochondrial permeability transition –> signal for apoptosis
membrane damage/increased permeability role in cell injury
ATP depletion, Ca activates phospholipases and direct damage by toxins/viral proteins/complement/perforins/chemical/physical agents
ROS role in cell injury
damage membranes, proteins and nucleic acids
dry gangrene causes
frostbite or intoxicants
wet gangrene causes
digested/liquified by environmental flora
two concurrent processes of necrosis
- enzymatic digestion
- protein denaturation
necrosis features
karyolysis
adjacent tissue unaffected
RBC intact
inflammation
passive, degradative
tissue response
membrane injury and organelle damage
causes of metastatic mineralization
hypervitamin D
renal disease
primary hyperparathyroidism
hyperadrenocorticism
paraneoplastic syndromes (PTHrP)
where is metastatic mineralization commonly found
gastric mucosa
blood vessels
lungs
kidney
are thrombi dystrophic or metastic mineralization
dystrophic due to presence of platelets and fibrin
apoptosis features
pyknosis & karyorrhexis
no inflammation
active process
no tissue response
DNA damage, no organelle damage
increased cytoplasmic eosinophilia
forms apopotic bodies
what intiiates apoptosis
extrinsic pathway
intrinsic pathway
perforin/granzyme pathway
increased apoptosis results in…
neurodegenerative disorders
exacerbation of damage in ischemic injury
virus-induced lymphocyte depletion in acquired immunity deficiency syndromes
decreased apoptosis results in…
neoplasia
autoimmune diseases
breakdown products of lipids, granular golden brown; usually microscopic
lipofuscin
dark, gross appearance, primarily in the lungs, urban environments, incidental
carbon
incidental pigmentation of tissues in pigmented animals; commonly affects pleura and meninges
melanin
postmortem production of hydrogen sulfide by bacteria with rxn with Fe in hemoglobin to form insoluble iron sulfide
pseudomelanosis
yellow pigment from wound, bruising
hematoidin
lighter brown granular pigment, represents accumulations of Fe & apoferritin
hemosiderin
greenish-brown pigment usually not granular, seen within hepatocytes/bile canaliculi/renal tubular epithelium; may be bright yellow and stain all tissues in hemolytic anemia (jaundice)
bilirubin
pinpoint hemorrhage, up to 1mm, capillary injury, petechiation
petechia
larger hemorrhage, up to a few cm, paintbrush appearance
ecchymosis
petechiae and ecchymoses on mucous membranes
purpura
focal hemorrhage which produced mass-like lesion
hematoma
causes of hemorrhage
local - trauma, hypoxia, degenerative conditions
systemic - coagulopathies, metabolic,, neoplastic, or infectious diseases
consequences of hemmorhage
primary - shock, space occupying lesions with disastrous consequences in CNS/pericardial sac
secondary - resorption of fluid, RBC lysis and phagocytosis, fibrinolysis, scarring
local edema causes
venous obstruction
lymphatic obstruction
inflammation or vascular injury
generalized edema causes
cardiac edema (increased hydrostatic pressure)
renal failure (decreased plasma oncotic pressure)
hepatic failure (decreased plasma oncotic pressure)
physioloical (eating, exercise) & pathological (inflammaltion/injury)
active hyperemia
pathological (heart failure, mechanical, gravity - recumbent animals)
passive hyperemia
acute passive hyperemia
sudden occlusion (torsion, strangulation)
anoxia
chronic passive hyperemia
long standing interference, not complete ischemia (heart failure)
hypoxia
best to worst fates of thrombi
fibrinolysis
organization and recanalization
propagation
embolism
antemortem clots vs postmortem
antemortem - attached to endothelium, lesion
postmortem - not attached to endothelium, incidental, no lesion
pale, dry, fibrin and platelets, firm thrombi
arterial thrombi
large, dark red, shiny, cranberry sauce-like thrombi with RBC
venous thrombi
a raised infarction is _______
acute
a depressed infarcation is _____
chronic
pale, light, anemic infarct is due to ____
arterial occlusion
dark, hemorrhagic infarct in tissues with dual circulation is due to _____
venous occlusion
how do you distinguish between an old infarct and new one
old has scar tissue, appears paler than adjacent tissue and smaller volume due to scarring
consequences of infarction
necrosis
which tissues are the most vulnerable to infarcts? least vulnerable?
most vulnerable - single perfusion organs - brain, heart, renal cortex
least vulnerable - dual blood supply organs - liver & lungs - must occlude both bronchial a. and pulmonary a. for lungs and both hepatic a. and portal v. for liver
pro-coagulant factors for hemostasis
endothelial cells only:
VWF
collagen
ADP and TXA2
tissue factor
Ca2+
clotting factors
platelet-activating factor
plasminogen activator inhibitor (PAI)
alpha2 antiplasmin
anti-coagulants factors for hemostasis
endothelial cells & blood proteins involved:
covering thrombogenic subendothelial collagen
NO and PGI2
Antithrombin III
Thrombomodulin
Plasminogen activators (t-PA and urokinase-like PA)
antithrombins & protein C&S
